Viral infections are the result of passive or active penetration of a virus and/or viral genome (ribonucleic acid or deoxyribonucleic acid) into a cell of an organism. Viral infection may also lead to subsequent propagation of the virus within the organism. The process of viral penetration into a cell requires overcoming the cell membrane typically. Some viral infection occurs by an endocytotic mechanism whereby an invagination of the cell membrane is created to form a vesicle (endosome) resulting in the passive uptake of the virus into the cell. Within the cell, the virus escapes from the endosome by fusion of the outer viral membrane with the membrane of the endosome. Alternatively, the virus actively injects the viral genome into the cytoplasm of the cell without itself entering into the cell. Both mechanisms ultimately lead to the entry of viral genome into the cytoplasm of the cell.
Viral penetration into the cell is usually followed by a propagation of the virus within the cell and subsequent release of the propagated virus from the cell. The released virus is subsequently capable of infecting further cells. A viral infection may be followed by a viral infectious disease, which manifests itself in terms of symptoms based on the viral infection.
Many attempts have been made to address viral infections by targeting particular components of the viral life cycle. Drugs that target viral replication within the cell represent a key inhibitory target mechanism in the field. Alternatively, some attempts have been made to target the mechanisms by which viruses enter a cell. For example, WO 2004/017949 attempts to prevent viral entry into a cell by disrupting ceramide-rich lipid rafts on the surface of cells. The reference attempts to use inhibitors of acid sphingomyelinase and/or inhibitors of ceramide or phosphorylcholine, products of the reaction catalyzed by this enzyme to alter the presence and characteristic of lipid rafts on the membrane surface.
Each of the viral targeting mechanisms of the past suffer significant drawbacks such as viral mutation leading to escape and reduced effectiveness of compositions, unwanted systematic or other side effects, the ability to target only a single virus type, or low success. As such, new compositions and mechanisms are needed for prophylaxis or treatment of viral infection.